Animal models of human memory disorders have shown that hippocampal cell loss results in contextual and spatial memory deficits, and that related, but distinctly different deficits result from the destruction of input fibers to the hippocampus (for example, entorhinal cortex lesions). It is still unclear if entorhinal cortex lesion deficits are due to a reduction in the sensory information reaching the hippocampus, or that the entorhinal itself is involved in contextual and spatial memory. Long-term memory consolidation requires gene expression and protein synthesis, mediated by signaling cascades and transcription factors. The Extracellular-signal Regulated Kinase (Erk) cascade has been shown to be necessary for several types of memory. It has been shown that fear conditioning and spatial tasks both activate the Erk cascade in the hippocampus and that long-term spatial memory storage is dependent on Erk activity in the dorsal hippocampus. My hypothesis is that the Erk cascade is necessary for certain aspects of contextual and spatial memory in both the entorhinal cortex and in the hippocampus. To test this hypothesis, we will characterize the nature of any behavioral deficits seen following Erk cascade inhibition in contextual and spatial tasks. The results generated will provide a new understanding of the structural and molecular basis of long-term memory storage.